bulbar and pseudobulbar palsy

[aspiringmd1015]

explan the differences please, wiki says bulbar is LMN, while pseudobulbar is UMN(corticobulbar tract damage), but its not verified.

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[Postictal Raiden]

According to the explanation in UW, bulbar palsy is caused by a lesion to cranial nerve nuclei while pseudobulbar is a demyelination of the nerves going from cortex to these nuclei. In other words, LMN vs UMN lesion, respectively.

 

[zhopv10]

Right so bulbar is damage of the facial nerve nuclei and distal: LMN. Pseudo bulbar can look similar but is damage to the descending fibers from the cerebrum (in the internal capsule/cerebral peduncle generally I thought not sure on that tho) but it is UMN.


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[aspiringmd1015]

so with the UMN(pseudobulbar) patient will present with uncontrolled activity of these nuclei? pathological laughter/crying etc?

 

[zhopv10]

Not usually sx's are often the same, they like to test the differences though (like if it is UMN in the cortex for CN VII then the forehead will be spared cause it's bilateral. Those types of differences are fairly high yield IMO


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[aspiringmd1015]

Not usually sx's are often the same, they like to test the differences though (like if it is UMN in the cortex for CN VII then the forehead will be spared cause it's bilateral. Those types of differences are fairly high yield IMO


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right, hypoglossal and contralteral lower face will be effected then, on wiki it sais something about pathologogical lafugher and crying etc. sorry for hte typos typing as quick as i can. do you know why sickled cells/t hallasemic cells are more resistant to hemolysis with hypotonic solutions

 

[zhopv10]

right, hypoglossal and contralteral lower face will be effected then, on wiki it sais something about pathologogical lafugher and crying etc. sorry for hte typos typing as quick as i can. do you know why sickled cells/t hallasemic cells are more resistant to hemolysis with hypotonic solutions

So I have t looked it up but I would suspect that it's because in spherocytosis there is an actual membrane defect that makes the cells not be able to deal with increase fluid coming in whereas in thalassemia it is small because you have a defect in hemoglobin that alters division numbers or whatever so they are micro cystic but those microcytic cell membranes are normal thus they can handle the increased fluid and distention ok.


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[aspiringmd1015]

okay sweet, thanks. any example of an uncompetitive inhibitor, which decreases KM and vmax?

 

[zhopv10]

honestly not sure on many, it seems they are kind of rare. lithium is apparently an example of it, some herbicides (roundup), some insecticides.